There are saturated fats, there are saturated fats, there are saturated fats, there are saturated fats, there are saturated fats and there are saturated fats. Saturated fats are an ester of Glycerol (a 3-carbon alcohol) and three saturated fatty acids (SFA's). There are roughly six categories of SFA's.

In foods, the above SFA's are associated with different things.
1) and 2) don't get associated with much polyunsaturated fatty acids (PUFA's), e.g. dairy and tropical nuts.
3) and 4) are more likely to be associated with long-chain PUFA's, e.g. meats, poultry, temperate nuts.
5) is associated with CLA and not much PUFA's, e.g. dairy from grass-fed animals.

Negative feedback control systems can overshoot, especially if there's a delay in the feedback path that's longer than the rise time of the input step.

An example of this is the first-phase insulin response. Loss of the first-phase insulin response occurs in over-fat people who are hyperinsulinaemic. Without the first-phase insulin response, there's a delay between an increase in blood glucose and an increase in insulin secretion. A rapid upwards step in blood glucose (say, from eating a high-GL meal) causes a massive overshoot in insulin secretion, resulting in postprandial sleepiness, also down-regulation of insulin receptor activity in the appetite centres of the brain, causing ravenous hunger when the insulin level falls to normal.

Wednesday, 25 June 2014

Li-i-ife, is the name of the game, and I wanna play the game with you.....

People have been "grinding my gears" by conflating carbohydrates with sugars. All sugars are carbohydrates, but not all carbohydrates are sugars. See Carbs Carbs Carbs. to find out about the five basic different types of carbohydrates.

In pseudoscience there’s a subtype called Denialism. Denialism seeks to deny an established science and violate multiple principles of logic, and scientific methodology, this is mostly because of a priori beliefs and preconceptions. Typically the same cognitive and logical errors are committed in denialism reasoning.

The whole process starts with a desired conclusion, that a generally accepted scientific or historical claim is not true. Denialists have ideological reasons, and engage in motivated reasoning, rationalizing away the undesired claim.

In essence and practical terms, they work backward from their desired conclusion, filling in justifications.

1. Moving the goalposts

In moving the goalposts, they always demand more evidence for a claim, even if currently available. However when that burden of evidence is met, the goalposts are moved and more evidence is demanded.

They may use vagueness in defining a certain term to move the goalpost away from any possible dis-confirming evidence.

2. Unreasonable demand for evidence

Because science has gaps, they explore them as if it the specific scientific theory being discussed is invalid or not well established.

Let’s take the example of HIV denial. Deniers often demand a single study or scientific paper establishing HIV as the cause of AIDS. However, it is not established by a single study but rather by a large body of evidence.

In scientific reasoning we must see if the gaps are slowly being filled, and if predictions are met, and if it fits together with other lines of evidence, observational or experimental.

If a theory has been going around in circles and not progressing, that is a strong indication of pseudoscience.

3. Pointing out disagreements

Disagreements within a discipline are explored, often small details, as if the science in question is not solid.

4. Denying entire categories of evidence

Another strategy the narrowing of evidence that may count as “scientific”. The most common is using the logical fallacy of confusing correlation with causation.

Correlation is not the same as causation, not necessarily anyway. Correlations need to be used properly, and multiple correlations can triangulate a specific causal relationship observed in a correlation. Epidemiology is based on correlations and observational evidence, if they were invalid the entire field simply would vanish.

They can even deny all historical sciences such as astronomy, geology, or even forensics.

5. False dichotomy

This is an argument from ignorance. If a version of events is not true then the alternate claim or version must be. However, they rarely provide positive evidence for their alternate claim.

6. Campaign of Doubt

Little factoids can be gathered and taken out of context. The goal is to sow doubt, uncertainty, and distrust, focusing on apparent inconsistencies, or gaps. However in healthy skepticism we consider all the evidence in the proper perspective, and even though knowledge is incomplete, reliable conclusions can be achieved.

7. Conspiracy theory

As a last resort comes the conspiracy theory, claiming that the scientific evidence itself is fraudulent, a grand conspiracy. This tactic allows them to dismiss all the evidence and rationalize it away.

Tuesday, 24 June 2014

Pseudoscience is so flawed that it cannot be considered legitimate science. Of course it is common to claim that one’s beliefs are scientific, but mostly they are not.

Pseudoscience lacks the true method of science and goes way beyond just a few errors, the methods themselves are so flawed that makes the theory suspicious.

Between the two extremes of science and pseudoscience there is a gray zone, but legitimate science and pseudosciences can still be identified. The denial of this two extremes in the continuum, is a false continuum logical fallacy, or philosophically called the demarcation problem.

Features of Pseudoscience

1. Motivated reasoning

The most prominent feature of this pathological science is working backward from desired results, or motivated reasoning. The result is that they make evidence fit into preconceived notions. They use biased logic and cherry-picked evidence in order to defend a desired conclusion. There’s no concern and effort to prove their own theories wrong.

This relates to the congruence bias, testing one’s own theory by looking for positive evidence and cherry-picked evidence.

2. Burden of proof and confirmation bias

They will only look for confirming evidence, avoid dis-confirming evidence, and may engage in special pleading and shifting the burden of proof.

In confirmation bias, they look for supportive evidence for their own desired conclusions, choosing only the evidence that supports their own theory, irrespective of quality, negative evidence.

3. Anecdotal evidence

Anecdotes are uncontrolled, or ad-hoc observations, and they are not systematic. They rely on confirmation bias and recall bias.

Low-grade evidence is often favored no matter how implausible it may be.

Emotional appeal is another typical tactic among pseudoscientists who try to defend their statements, claiming what people say is more important than actual numbers on paper.

Pseudoscientific belief may even be based upon a single case or observation, preliminary evidence, or even a single anecdote. This is the hasty generalization logical fallacy.

Pseudoscientific principles may also be based upon a philosophical idea, not been empirically tested or developed as a scientific theory.

4. Grandiose claims (Galileo syndrome)

This involves grandiose claims based upon preliminary evidence. Far-reaching claims overturn entire portions of well-established science, using very little research or tiny bits of evidence.

5. Alternative science

In extreme cases, pseudoscience leads to alternative science, all of science is replaced with an alternative version.

6. Absolute claims

Pseudoscientists make bold claims that are often absolute and go way beyond the evidence. Pseudoscientists offer simple answers to complex questions, a theory of everything where one tiny casual source is used to explain the entire universe, if it comes to that.

7. Hostility

Pseudoscientists generally cannot accept criticism and avoid the scientific community. They claim being victim of a conspiracy and stay away from mainstream science and community.

8. Vagueness

Pseudoscientists use vague terms and words to obfuscate, so they can shift the definition around, use it in different ways at different times when it suits them, to confuse others and avoid explaining their point. Vague terms such as “information” or “energy” are often used with no specificity as in a scientific discussion.

9. Stagnation

Pseudosciences fail to progress, and tend to be stagnant. They are ad nauseam trying to establish their theory rather than build a body of evidence for it.

10. Anomaly hunting

Anomaly hunting is yet another common feature in which they search for anomalies trying to establish a conclusion, which does not seek to refute or explore other alternatives.

Chronic excessive consumption of carbohydrates relative to what are being burned results in excessive fat synthesis in the liver, resulting in excessively-high fasting serum triglyceride level, which is harmful.

Chronic excessive consumption of fats relative to what are being burned results in excessive cholesterol synthesis in the liver, resulting in excessively-high fasting VLDL, LDL & IDL level, which is harmful.

The results from Pietinen et al are statistically-insignificant (95% CI values are way above & below 1) with an overall slight protective effect. The results from Mann et al have a RR >> 1 with both 95% CI's >1 and the results from Boniface et al have a RR >1 with both 95% CI's >1.

Other studies either have sat fat intakes varying from very low to low, or specify mean/median sat fat intakes without values for highest & lowest tertiles/quartiles/quintiles etc. Other studies have results that are statistically-insignificant.

However, there are some studies that show a slight protective effect of small amounts of sat fats. How come?

HRs and 95% CI's of CVD risk according to quintiles of energy-adjusted SF from different sources (n = 5209).

The Meat SF plot has a net positive slope (bad news, but the range of intake is very small), the Butter & Plant SF plots are random, but the Dairy SF plot has a net negative slope (good news). Dairy saturated fats in amounts of up to 10g/day are protective against CHD. As the Dairy sat fat intake is too small to have a significant effect on lipids, what's the mechanism? I think that it's Vitamin K2. See Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.

When you average out the results from all studies, the result is null. This is data dilutionstatistics.

Notice how the HR falls with increasing time from last meal. As TG's ≥12 hours after eating are a surrogate for Insulin Resistance (IR) and the HR is only 1.04 (95% CI 0.79 - 1.38), this strongly suggests that IR is not a significant factor.

Second, the reason why I'm having to repeat myself is due to Cholesterol: Do chylomicrons clog your arteries? (2), where I've been called "my resident lipophobe". As I drink Gold Top milk (5.2g of fat/100mL) and eat pork including belly slices (you know, those strips of pork with a lot of fat on them), I'm being attacked for something that I'm not.

What I'm criticising is dietary extremism. Eating fats in foods is fine by me, but eating sticks of Kerrygold butter and/or dumping loads of butter and/or MCT oil into coffee to achieve "Nutritional Ketosis" is not a good idea. Anyway, here's an amusing spoof on Bulletproof coffee.

Thursday, 12 June 2014

Carbohydrates seem to get the blame for everything nowadays. "Carbohydrates made me fat". "Carbohydrates burned-out my pancreas". "Carbohydrates raised my blood glucose". "Carbohydrates raised my blood triglycerides". "Carbohydrates stole mer jerb!". O.K, I made the last one up!
If carbohydrates are responsible for all of these bad things, then how come a diet of only potatoes had the opposite effect? See 20 Potatoes a day.

The experimental diet which did bad things contained 37.5%E from sugars. I declare shenanigans!

1. There are simple carbs, there are simple carbs and there are simple carbs. In the previous post, the graph of plasma triglycerides after an OGTT showed that 100g of glucose had no significant effect on plasma triglycerides over a 6 hour period. If it had been 100g of fructose, there would have been a significant increase in plasma triglycerides. Galactose is taken-up by the liver and has minimal effect on blood glucose, but I don't know its effect on plasma triglycerides.

2. There are complex carbs, there are complex carbs and there are complex carbs. Overcooked starch is high in amylopectin which is highly-branched, which means that it hydrolyses rapidly into glucose which gives it a very highglycaemic index. Raw & refrigerated potato starches have very low glycaemic indices, due to the presence of amylose, or other resistant starches. Rice contains a mixture of starches which varies with rice type, cooking time and subsequent refrigeration.

Wednesday, 11 June 2014

Fat storage:

Here's a plot of mean (±SEM) plasma insulin concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal.

100g of glucose produces a large spike in insulin concentration and 40g of fat produces no significant spike in insulin concentration. According to Gary Taubes' insulin hypothesis of obesity, in the absence of a significant spike in insulin concentration, fat cannot be stored.

Here's a plot of mean (±SEM) plasma triacylglycerol concentrations
during an oral-fat-tolerance test (OFTT) when preceded by either a
high-fat (•) or a high-carbohydrate (○) evening meal (from the previous post).

At a fat-burning rate of ~0.11g/min, it would take ~360min for plasma triacylglycerol to fall to baseline if the 40g of fat from the OFTT was only being burned and not being stored. As shown above, it only takes ~120min to fall to baseline. Therefore, fat from the OFTT that isn't burned is stored in ~120min in the absence of a significant insulin spike. Q.E.D.

A delicious analogy:

Here's a plot of mean (±SEM) plasma glucose concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (from the previous post).

The OGTT (100g of glucose) produces a large spike in plasma glucose concentration which lasts for ~210min before returning to baseline. Higher plasma glucose concentrations glycate more than lower plasma glucose concentrations. Average plasma glucose concentration over 0 to 360min is higher with the OGTT than with the OFTT, therefore there is more glycation damage with the OGTT than with the OFTT. Don't regularly consume 100g or more of glucose!

Here's a plot of Mean (±SEM) plasma triacylglycerol concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal.

Average plasma triacylglycerol concentration over 0 to 360min is ~1.0mmol/L (~89mg/dL in US units).

Although the plasma triacylglycerol concentration after consuming a high-carbohydrate evening meal is slightly higher than after consuming a high-fat evening meal, the two plots above are essentially flat, indicating that none of the 100g of glucose consumed was turned into fat by de novo lipogenesis (DNL) within 6 hours.

As discussed in the previous post, higher plasma triacylglycerol concentrations are more atherogenic than lower plasma triacylglycerol concentrations. Average plasma triacylglycerol concentration over 0 to 360min is higher with the OFTT than with the OGTT, therefore there is more atherogenicity with the OFTT than with the OGTT.
Don't regularly consume 40g or more of fat!

An interesting study that involved humongous fat consumption was Response of body weight to a low carbohydrate, high fat diet in normal and obese subjects , which used up to 600g of fat/day. It's possible to lose weight on an ultra-high-fat diet, but average plasma triacylglycerol concentrations would have been extremely high. Fasting TG's reduce on an ultra-high-fat diet, probably due to suppression of endogenous TG synthesis by exogenous TG intake.

Tuesday, 10 June 2014

The good:

Here's a plot of mean (±SEM) plasma glucose concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal.

An OFTT (40g of fat as cream) causes a significant rise in blood triacylglycerol (a.k.a. TAG a.k.a. triglycerides a.k.a. TG's) level for up to 4 hours. Note that the effect of a preceding high-carbohydrate meal on fasting TG's is only +0.1mmol/L. Is high postprandial TG's a problem? Definitely, maybe. From Cholesterol And Coronary Heart Disease , "Cholesterol-depleted particles oxidise faster than large, cholesterol-rich ones." Chylomicrons, chylomicron remnants & VLDL-C are triglyceride-rich, cholesterol-poor, as that's the composition of the fat in the diet.

A counter-argument is that the subjects in the above studies were eating carbohydrate, and that postprandial TG's aren't atherogenic if you're not eating much carbohydrate. Definitely, maybe. In the absence of carbohydrate, there is still glucose in the blood, thanks to the liver. Also, some carbohydrates don't spike blood glucose (or fructose) level. It's pure speculation that the subjects in the above studies had high blood glucose at the same time as high postprandial TG's. As Insulin Resistance/Metabolic Syndrome and/or a high-sugar diet raise fasting TG's, and there was no significant association between fasting TG's and the risk factor for CHD, this suggests that the subjects had no significant metabolic derangement and were not eating excessive amounts of sugar.

It's possible to get Coronary Artery Calcium (CAC) scans, to measure the amount of calcified plaque in coronary arteries. While a high CAC value means lots of plaque, a zero CAC value doesn't necessarily mean zero plaque, as young people and people with a high Vitamin K2 intake don't have significant calcification. See Stenosis Can Still Exist in Absence of Coronary Calcium.

Saturday, 7 June 2014

EDIT: I made an error in stating that all of the extra calories came from fat, in the fat overfeeding phase. Thanks to commenter CynicalEng for pointing that out. It doesn't change the conclusion at all.

At 02:22, I replied:-
"Thanks for that. I read Feinman's blog post about Bray et al http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777747/ some time ago.There's a fundamental error in Feinman's analysis. As LeonRover pointed out in his comment http://feinmantheother.com/.../bray-et-al-shows-that.../...
In Diets:- "Absolute carbohydrate intake was kept constant throughout the study."
Also, in COMMENT:- "The extra calories in our study were fed as fat, as in several other studies, and were stored as fat..."
Oh, whoops! That may be why it was rejected by the editor."

∴ A calorie *is* a calorie (where weight change is concerned) ± some inter-personal variation.∴Insufficient protein can result in LBM loss (this is bad).
As LBM has a lower Energy Density (~600kcals/lb) than FM (~3,500kcals/lb), LBM loss can increase weight loss, when in a Caloric Deficit.
See The Energy Balance Equation, for a simple explanation, and The Dynamics of Human Body Weight Change, for an incredibly complicated one!

I was rather chuffed when Alan Aragon left the following comment at 04:34:-
"Nigel is correct. From Bray et al's text:
"The extra calories in our study were fed as fat, as in several other studies [33,34], and stored as fat with the lower percentage of excess calories appearing as fat in the high (25%) protein diet group. The higher fat intake in the low protein group probably reduced nutrient absorption (metabolizable energy) relative to the other groups and this would have brought the intake and expenditure closer together in this group.""

Dr. George A. Bray used a "weight maintenance formula" in all three groups for the weight maintenance phase. He then changed the formula in all three groups to low-P, med-P and high-P formulas, for the fat overfeeding phase. Carbohydrate grams remained constant in all three groups for all phases, but additional fat grams were fewer in the high-P group than in the low-P group, for the fat overfeeding phase.

I would have used the low-P, med-P and high-P formulas for the weight maintenance phase and for the fat overfeeding phase, to equalise the additional fat grams in all three groups.

Monday, 2 June 2014

Some people believe that hormonal disruption causes obesity, rather than energy excess. The vast majority of people who are overweight or obese weren't born with hormonal disruption. It's years of chronic energy excess (see Determinants of the Variability in Human Body-fat Percentage for the many reasons causing it) that make people too heavy/fat than is healthy. Once too heavy/fat than is healthy, various hormones become disrupted, causing even more energy excess. Therefore, the cause of obesity is not one thing or another, it's both (plus lots of others), which is why reversing it is so difficult.

On Peter D's blog, the title reads "You need to get calories from somewhere, should it be from carbohydrate or fat?" I say "Both. And some protein. And a bit of alcohol, too!" And I know that I shouldn't start sentences with And.

It's been a while since I posted a video of me singing. Here's one from February this year.

About Me

I have a B.Sc.(Hons) in Electronic Engineering but no qualifications in Diet, Nutrition & Fitness, which is why I back-up what I write with links to high-quality evidence.

You can email me at
nigel.kinbrum@entee'ellworld.com
(say it!).

My suggestions must ALWAYS be checked by your Pharmacist/GP first, in case of contraindications with other medical conditions or medications that I don't know about. My suggestions are adjuncts to, NOT replacements for medication(s).

If symptoms improve, ask your GP about a reduction in medication(s), if it's/they're causing you problems.

Cheers, Nigel Kinbrum B.Sc.(Hons)Eng.

Moderation Policy:-READ THIS BEFORE COMMENTING. I can approve comments using my phone when I'm away from my lap-top, but I prefer to type replies on my lap-top, so please be patient.

Competing Interest:- When you get a $5 discount by using code NIG935 on iHerb.com, I get a $5 reward.